Myocardial ischemia/reperfusion (I/R) injury contributes to the pathogenesis of numerous diseases. Based on its antioxidant and anti‑inflammatory effects, dimethyl fumarate (DMF) has been reported to exert protective effects against I/R. However, to the best of our knowledge, its potential role as a myocardial protective agent in heart disease has received little attention. Previous studies have suggested that DMF may exert its protective effects by activating nuclear factor erythroid 2‑related factor 2 (Nrf2); however, the exact underlying mechanisms remain to be elucidated. The aim of the present study was to investigate the protective role of DMF in myocardial I/R injury, and to determine the role of Nrf2 in mediating the activity of DMF. H9c2 cells were incubated with DMF (20 µM) for 24 h before establishing the I/R model, and were then subjected to myocardial ischemia for 6 h, followed by reperfusion. Cell viability, lactate dehydrogenase levels, anti‑oxidant enzyme expression levels and anti‑apoptotic effects were evaluated, and AKT/Nrf2 pathway‑associated mechanisms were investigated. The results of the present study indicated that DMF may reduce myocardial I/R injury in a Nrf2‑dependent manner. DMF significantly improved cellular viability, suppressed the expression of apoptotic markers, decreased the production of reactive oxygen species and increased the expression of Nrf2‑regulated antioxidative genes. Notably, these beneficial DMF‑mediated effects were not observed in the control or I/R groups. In conclusion, the results of the present study suggested that DMF may exert protective effects against a myocardial I/R model, and further validated Nrf2 modulation as a primary mode of action. Thus suggesting that DMF may be a potential therapeutic agent for AKT/Nrf2 pathway activation in myocardial, and potentially systemic, diseases.Osteoporosis is a systemic metabolic bone disease during which bone mass decreases and bone quality is reduced. Maintaining the bone formation capacity of osteoblasts is crucial for the treatment of osteoporosis. In the present study, bioinformatics analysis was performed on online microarray expression profiles to identify miRNA(s) related to osteoblast proliferation and bone marrow‑derived mesenchymal stem cell (BMSC) osteogenic differentiation. The specific effects of candidate miRNAs on cell proliferation, osteogenic differentiation and Wnt signaling‑related factors were examined. As regards the downstream mechanisms, online tools were employed to predict the downstream targets of candidate miRNAs and the predicted miRNA‑mRNA binding was verified. Finally, the dynamic effects of miRNAs and mRNAs were examined. The results revealed that miR‑483‑3p expression was decreased in bone tissue samples from patients with osteoporosis. In miR‑483‑3p‑overexpressing human osteoblasts, cell viability, DNA synthesis capacity and osteogenesis were promoted, and the protein levels of Wnt1, β‑catenin and cyclin D1 were increased. However, the protein receptor activator of nuclear factor kappa‑Β ligand (RANKL)/osteoprotegerin (OPG) ratio and cell apoptotic rate were decreased. The Wnt signaling, antagonist Dikkopf 2 (DKK2), was targeted and negatively regulated by miR‑483‑3p. DKK2 knockdown exerted similar effects as miR‑483‑3p overexpression, while DKK2 overexpression inhibited cell viability, DNA synthesis capacity and osteogenesis. DKK2 overexpression also decreased the Wnt1, β‑catenin, and cyclin D1 protein levels, whereas it promoted the the RANKL/OPG ratio and the apoptosis of human osteoblasts. DKK2 overexpression reversed the functions of miR‑483‑3p overexpression. On the whole, the findings of the present study demonstrate that the miR‑483‑3p/DKK2 axis modulates the bone formation process by affecting osteoblast proliferation, pre‑osteoblast differentiation into mature osteoblasts and new bone matrix formation.Subsequently to the publication of the above paper, the authors have realized that the western blots featured in Fig. 5B were inadvertently copied across from Fig. 4B owing to an error made during the figure compilation process. The corrected version of Fig. 5 is featured on the next page, showing the correct data for the western blot analysis of the programmed death receptor ligand 1 level in radioresistant lung cancer cells under the specified experimental conditions. Note that these changes do not affect the interpretation of the data or the conclusions reported in this paper, and all the authors agree to this correction. The authors apologize to the Editor and to the readership of the Journal for any inconvenience caused. VY-3-135 [the original article was published in International Journal of Oncology 53 317-328, 2018; DOI 10.3892/ijo.2018.4394].Following the publication of this article, the authors have realized that the affiliation for the first author, Huashan Huang, was presented incorrectly as a multiple affiliation Because the student was under the supervision of Professor Pengli Zhu, the only affiliation that should have been presented in this paper for this author was for the first affiliation, i.e., Shengli Clinical Medical college of Fujian Medical University. Therefore, the author affiliations for this paper should have appeared as follows HUASHAN HUANG1, HUIZHEN YU1-3, LIANG LIN4, JUNMING cHEN1,2 and PENGLI ZHU1,2 1Shengli Clinical Medical College of Fujian Medical University; 2Key Laboratory of Geriatrics, Fujian Provincial Hospital, Fuzhou, Fujian 350001; Departments of 3Cardiology and 4Gynecology and Obstetrics, Fujian Provincial Hospital South Branch, Fuzhou, Fujian 350028, P.R. China. [the original article was published in International Journal of Molecular Medicine 45 1864-1874, 2020; DOI 10.3892/ijmm.2020.4542].Mostotrin (MT), a novel compound, at least five orders of magnitude more soluble in water than its mother substance, was designed and synthesised from tryptanthrin (TR). Its structure was established by nuclear magnetic resonance and mass spectrometry data and confirmed by X‑ray analysis, revealing that MT is a pentacyclic product with an additional pseudo‑cycle formed with the participation of one intramolecular hydrogen bond. Antimicrobial activity and cytotoxic action against tumour cells in vitro, as well as anti‑tumour effects, acute toxicity and anti‑inflammatory activities in vivo, were evaluated. Antimicrobial properties of MT against Mycobacterium spp and Bacillus cereus ATCC 10702 appeared to be the same as that of TR, but against the other strains used it was weaker. Furthermore, MT exhibited 5‑10 times higher cytotoxic activities against tumour cell lines HCT‑116, МСF‑7 and K‑562 than TR, but was less toxic than TR (LD50 of MT was 375 mg/kg, while LD50 for TR was 75 mg/kg). Additionally, compounds MT and TR were studied in DNA binding tests.